Evidence map›Paper›PMID 39674501›Full record

ArticleJournal of advanced research2025

CD34

Xin-Yu Zhu, Wen-Ting Liu, Xiao-Juan Hou, Chen Zong, Wei Yu, Zhe-Min Shen, Shu-Ping Qu, Min Tao, Meng-Meng Xue, Dao-Yu Zhou and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Regulation of Cancer Stem Cells in the Tumor Microenvironment.Cancer heterogeneity and plasticity · 2025
    Article
  10. Review
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Xin-Yu ZhuChanghai Clinical Research Unit, Changhai Hospital of Naval Medical University, Shanghai, China; Tumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Wen-Ting LiuTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China; Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Xiao-Juan HouTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Chen ZongTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Wei YuChanghai Clinical Research Unit, Changhai Hospital of Naval Medical University, Shanghai, China; Tumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Zhe-Min ShenTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Shu-Ping QuDepartment of Hepatic Surgery, Third Affiliated Hospital of Naval Medical University, Shanghai, China.
Min TaoChanghai Clinical Research Unit, Changhai Hospital of Naval Medical University, Shanghai, China; Department of Clinical Pharmacology, The Second Hospital of Anhui Medical University, Hefei, China.
Meng-Meng XueChanghai Clinical Research Unit, Changhai Hospital of Naval Medical University, Shanghai, China; Department of Clinical Pharmacology, The Second Hospital of Anhui Medical University, Hefei, China.
Dao-Yu ZhouChanghai Clinical Research Unit, Changhai Hospital of Naval Medical University, Shanghai, China; Tumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Hao-Ran BaiDepartment of Oncology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Lu GaoTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Jing-Hua JiangTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Qiu-Dong ZhaoTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Li-Xin WeiTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China.
Xue YangTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China. Electronic address: yangxue19900307@126.com.
Zhi-Peng HanTumor Immunology and Metabolism Center, National Center for Liver Cancer, Naval Medical University, Shanghai, China; Department of Oncology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address: hanzhipeng0311@126.com.
Li ZhangChanghai Clinical Research Unit, Changhai Hospital of Naval Medical University, Shanghai, China. Electronic address: lizhangpaper@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe heterogeneity of hepatocellular carcinoma (HCC) is linked to tumor malignancy and poor prognosis. Nevertheless, the precise mechanisms underlying the development of the cholangiocellular phenotype (CCA) within HCC remain unclear. Emerging studies support that the cross-talk among the host cells within tumor microenvironment (TME) sustains the cancer cell plasticity.

objectivesThis study sought to identify the specific cell types involved in the formation of CCA and to elucidate their functional roles in the progression of HCC.

methodsSingle-cell RNA sequencing was employed to identify the specific cell types involved in the formation of CCA. Both in vitro and vivo analyses were used to identify the tumor-associated senescent ECs and investigate the function in TME. The diethylnitrosamine-induced model was utilized to investigate the interaction between senescent ECs and MSCs, aiming to elucidate their synergistic contributions to the progression of CCA.

resultsUsing single-cell RNA sequencing, we identified a distinct senescent-associated subset of endothelial cells (ECs), namely CD34

conclusionsTogether, our findings illustrated that tumor associated senescent ECs in HCC recruited the MSCs into TME, enhancing cancer stem cell (CSC)-like features of HCC cells and contributing to the CCA formation.

Indexed as

Carcinoma, HepatocellularCholangiocarcinomaEndothelial CellsInsulin-Like Growth Factor IILiver NeoplasmsAnimalsAntigens, CD34Cell Line, TumorCellular SenescenceHumansMaleMesenchymal Stem CellsMicePhenotypeSignal TransductionTumor MicroenvironmentAntigens, CD34IGF2 protein, humanInsulin-Like Growth Factor IICholangiocellular phenotypeMesenchymal stem cellsSingle-cell RNA sequencingTumor associated senescent endothelial cells

Identifiers

PMID39674501
PMCPMC12793740

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.